What does this research mean for the field?

Atrial fibrillation induces similar structural remodeling in men and women, though female patients exhibit a significantly higher upregulation of the gap junction protein connexin40. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

January 11, 2013

Gender-Specific Remodeling in Atrial Fibrillation?

Key Result

This document is a journal masthead and contains no clinical study data.

Structured PICO

Does gender influence the atrial remodeling process (gap junction proteins, collagen I, amyloid) in patients with atrial fibrillation?

Population

123 patients with sinus rhythm (n=41) or atrial fibrillation (n=82) suffering from mitral valve disease undergoing cardiac surgery.

Intervention

Atrial fibrillation (observational comparison by gender)

Comparator

Sinus rhythm (and male vs female comparison)

Outcome

Expression of atrial gap junction proteins (Cx40, Cx43), collagen I, and amyloid depositionssurrogate

Atrial remodeling in AF is largely similar between men and women, though women may exhibit slightly stronger AF-induced changes in Cx40 expression.

Abstract

BACKGROUND: The authors wanted to investigate whether the remodeling process in AF regarding gap junction proteins, collagen I, and amyloid may be gender dependent in humans. METHODS: In total, 123 patients with sinus rhythm (SR, n = 41) or atrial fibrillation (AF, n = 82) suffering from mitral valve disease undergoing cardiac surgery were included. Of the 123 patients, 66 patients (SR: n = 17, AF: n = 49) were investigated biochemically for the expression of the atrial gap junction proteins connexin40 (Cx40), connexin43 (Cx43) and collagen I and 57 patients (SR: n = 24; AF: n = 33) using histochemical methods for possible amyloid depositions. RESULTS: AF led to increased levels of Cx40, Cx43, and collagen I protein. Regarding Cx40 this upregulation was significantly higher in female than in male patients. For AF-induced changes in collagen or Cx43, there were no significant gender-dependent differences. Amyloid depositions were found with increasing age, but were not significantly related to AF or gender. CONCLUSIONS: Remodeling in AF seems to be similar in men and women, with a tendency for women exhibiting somewhat stronger AF-induced changes in Cx40, which is probably a secondary effect because there is nothing known about hormone sensitivity of the Cx40 promoter, and a not significant tendency for higher Cx43 and collagen I.

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